Treatment-associated polymorphisms in protease are significantly associated with higher viral load and lower CD4 count in newly diagnosed drug-naive HIV-1 infected patients |
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| Authors: | Kristof Theys Koen Deforche Jurgen Vercauteren Pieter Libin David AMC van de Vijver Jan Albert Birgitta ?sj? Claudia Balotta Marie Bruckova Ricardo J Camacho Bonaventura Clotet Suzie Coughlan Zehava Grossman Osamah Hamouda Andrzei Horban Klaus Korn Leondios G Kostrikis Claudia Kücherer Claus Nielsen Dimitrios Paraskevis Mario Poljak Elisabeth Puchhammer-Stockl Chiara Riva Lidia Ruiz Kirsi Liitsola Jean-Claude Schmit Rob Schuurman Anders S?nnerborg Danica Stanekova Maja Stanojevic Daniel Struck Kristel Van Laethem Annemarie MJ Wensing Charles AB Boucher Anne-Mieke Vandamme |
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| Affiliation: | 1. Department of Microbiology, University of Iowa, Carver College of Medicine, Iowa City, IA, USA
2. Department of Microbiology, Carver College of Medicine, University of Iowa, Iowa City, IA, 52242, United States of America
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| Abstract: | Background Bone marrow stromal cell antigen 2 (BST-2) is a cellular factor that restricts the egress of viruses such as human immunodeficiency virus (HIV-1) from the surface of infected cells, preventing infection of new cells. BST-2 is variably expressed in most cell types, and its expression is enhanced by cytokines such as type I interferon alpha (IFN-??). In this present study, we used the beta-retrovirus, mouse mammary tumor virus (MMTV) as a model to examine the role of mouse BST-2 in host infection in vivo. Results By using RNA interference, we show that loss of BST-2 enhances MMTV replication in cultured mammary tumor cells and in vivo. In cultured cells, BST-2 inhibits virus accumulation in the culture medium, and co-localizes at the cell surface with virus structural proteins. Furthermore, both scanning electron micrograph (SEM) and transmission electron micrograph (TEM) show that MMTV accumulates on the surface of IFN??-stimulated cells. Conclusions Our data provide evidence that BST-2 restricts MMTV release from naturally infected cells and that BST-2 is an antiviral factor in vivo. |
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